C9orf72-Associated Dipeptide Repeat Expansions Perturb ER-Golgi Vesicular Trafficking, Inducing Golgi Fragmentation and ER Stress, in ALS/FTD
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- Extent
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1 Online-Ressource.
- Language
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Englisch
- Bibliographic citation
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C9orf72-Associated Dipeptide Repeat Expansions Perturb ER-Golgi Vesicular Trafficking, Inducing Golgi Fragmentation and ER Stress, in ALS/FTD ; day:9 ; month:5 ; year:2024 ; pages:1-21
Molecular neurobiology ; (9.5.2024), 1-21
- Creator
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Sultana, Jessica
Ragagnin, Audrey M. G.
Parakh, Sonam
Saravanabavan, Sayanthooran
Soo, Kai Ying
Vidal, Marta
Jagaraj, Cyril Jones
Ding, Kunjie
Wu, Sharlynn
Shadfar, Sina
Don, Emily K.
Deva, Anand
Nicholson, Garth
Rowe, Dominic B.
Blair, Ian
Yang, Shu
Atkin, Julie D.
- Contributor
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SpringerLink (Online service)
- DOI
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10.1007/s12035-024-04187-4
- URN
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urn:nbn:de:101:1-2407190817566.674207219562
- Rights
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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14.08.2025, 10:55 AM CEST
Data provider
This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Sultana, Jessica
- Ragagnin, Audrey M. G.
- Parakh, Sonam
- Saravanabavan, Sayanthooran
- Soo, Kai Ying
- Vidal, Marta
- Jagaraj, Cyril Jones
- Ding, Kunjie
- Wu, Sharlynn
- Shadfar, Sina
- Don, Emily K.
- Deva, Anand
- Nicholson, Garth
- Rowe, Dominic B.
- Blair, Ian
- Yang, Shu
- Atkin, Julie D.
- SpringerLink (Online service)
Other Objects (12)
ALS/FTD-associated mutation in cyclin F inhibits ER-Golgi trafficking, inducing ER stress, ERAD and Golgi fragmentation
Golgi
CUG initiation and frameshifting enable production of dipeptide repeat proteins from ALS/FTD C9ORF72 transcripts
Dipeptide repeat proteins inhibit homology-directed DNA double strand break repair in C9ORF72 ALS/FTD
The Golgi apparatus
Fragmentation of Golgi complex and Golgi autoantigens during apoptosis and necrosis
Golgi apparatus and Golgi outposts in neurons studied by correlative microscopy
Poly‐ GP in cerebrospinal fluid links C9orf72 ‐associated dipeptide repeat expression to the asymptomatic phase of ALS/FTD
TDP43 aggregation at ER-exit sites impairs ER-to-Golgi transport
In focus Golgi apparatus
Golgi, Camillo (1843-1926)
Giantin is the major Golgi autoantigen in human anti-Golgi complex sera
ALS/FTD-associated mutation in cyclin F inhibits ER-Golgi trafficking, inducing ER stress, ERAD and Golgi fragmentation
Golgi
CUG initiation and frameshifting enable production of dipeptide repeat proteins from ALS/FTD C9ORF72 transcripts
Dipeptide repeat proteins inhibit homology-directed DNA double strand break repair in C9ORF72 ALS/FTD
The Golgi apparatus
Fragmentation of Golgi complex and Golgi autoantigens during apoptosis and necrosis
Golgi apparatus and Golgi outposts in neurons studied by correlative microscopy
Poly‐ GP in cerebrospinal fluid links C9orf72 ‐associated dipeptide repeat expression to the asymptomatic phase of ALS/FTD
TDP43 aggregation at ER-exit sites impairs ER-to-Golgi transport
In focus Golgi apparatus
Golgi, Camillo (1843-1926)
Giantin is the major Golgi autoantigen in human anti-Golgi complex sera
ALS/FTD-associated mutation in cyclin F inhibits ER-Golgi trafficking, inducing ER stress, ERAD and Golgi fragmentation
Golgi
CUG initiation and frameshifting enable production of dipeptide repeat proteins from ALS/FTD C9ORF72 transcripts
Dipeptide repeat proteins inhibit homology-directed DNA double strand break repair in C9ORF72 ALS/FTD
The Golgi apparatus
Fragmentation of Golgi complex and Golgi autoantigens during apoptosis and necrosis
Golgi apparatus and Golgi outposts in neurons studied by correlative microscopy
Poly‐ GP in cerebrospinal fluid links C9orf72 ‐associated dipeptide repeat expression to the asymptomatic phase of ALS/FTD
TDP43 aggregation at ER-exit sites impairs ER-to-Golgi transport
In focus Golgi apparatus
Golgi, Camillo (1843-1926)